Osteoarthritis

Osteoarthritis – most common type of joint disease

Characterized by the progressive erosion of articular cartilage.
Though osteoarthritis implies an inflammatory disease, "OA is considered to be an intrinsic disease of cartilage in which biochemical and metabolic alterations result in its breakdown."
80-90% of people have evidence of OA by age 65. 80% of all joint replacement done for OA.
OA vs Aging: at 35, risk increases exponentially

Primary OA – Slow onset, no apparent initiating cause, aging phenomenon. Usually oligoarticular (affects few joints) but may be generalized. Note: 25-30% of patients with OA have a family history.

Secondary OA – 5% of cases with predisposing conditions, repeated injuries to joint, congential join deformity, diabetes, hemochromatosis, marked obesity. Usually one or several predisposed joints.
Knees, hands in women
Hips in men

Pathogenesis

Changes in proteoglycans and collagen, which decrease tensile strength and shorten fatigue life.

But OA is more than just cartilage wear-and-tear.

Chondrocytes play big role. Make IL-1 and TNF-a Þ Ý catabolic metalloproteniase synthesis, ß collage II and proteoglycan synthesis. Note: even though proteoglycans can be quickly replenished by chondrocytes, collagen production takes a long time and thus destruction will exceed production!!!

Cytokines also attract inflammatory cells.

Precise events that lead to secretion of cytokines is unclear.

Histology

Cartilage wears away, underlying cancellous bone scleroses, pieces of cartilage and subchondral bone dislodge into joint forming loose bodies (joint mice). Synovial fluid forced into fracture gaps, loculated fluid collection increases in size forming fibrous walled cysts. Mushroom-shaped osteophytes (bony outgrowths) develop at margins of articular surface and are capped by fibrocartilage and hyaline cartilage that gradually ossify. Osteophytes are the hallmark of the disease, they develop as a protective mechanism (to provide more support for the cartilage-less bone) but can become problematic. Synovium becomes congested and fibrotic and may have scattered chronic inflammatory cells.

cartilage breakdown Þ increase in fibers and proteoglycans; loss of collagen (cannot rebuild)

loss of joint space: erosions, spurs, osteophytes

In severe disease a fibrous synovial pannus covers the peripheral potions of the articular surface.

Clinical Manifestations

Insidious disease.

Deep, achy pain that worsens with use, morning stiffness, limitation of range of movement, joint tenderness and swelling. Osteophytes may impinge on spine (cervical/lumbar nerve root compression) causing pain, muscle spasms, muscle atrophy, and neurologic deficits.

Joints commonly involved – hips, knees, lower lumbar and cervical vertebrae, proximal and distal interphangeal joints, first carpometacarpal joints, and first tarsometatarsal joints of feet.

In women: Heberden nodes in fingers – osteophytes at DIP joints.

(if no PIP involvement, but PIP and MP involvement Þ Rheumatoid arthritis)

Why does disease only affects some joints? Possibility is variable gene expression in different joints.

Diagnosis and Treatment

Labs: No specific diagnostic test exists.

No prevention

No halting of progression

Treatment: Disease understanding, joint rest, physical therapy, analgesic agents (COX-2 inhibitors), anti-inflammatory agents, surgery.

Injections of hyaluronic acid may give some symptomatic relief.
Doxycycline – antibiotic that may inhibit collagenase enzymes.

	Osteoarthritis	Rheumatoid arthritis
Where it originates	Articular Cartilage	Synovium
Joints	weight bearing (hips, knees, back) PIP and DIP (also MP and TP)	hands, feet, wrists, elbow
Histology	chondrocyte clustering metachromasia fibrillation (flaking) subchondral thickening subchondral cysts	synovitis leading to edema, vascular proliferation, inflammatory infiltrates, Pannus